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PubMedDate not supplied

Failure of propranolol to prevent chronic hyperthyroid induced cardiac hypertrophy and multifocal cellular necrosis in the rat.

The effect of excess thyroid and thyroid plus propranolol on right and left ventricular structure was examined. Perfusion fixed hearts from untreated adults and those treated for 10 weeks with thyroid, propranolol, and thyroid plus propranolol were embedded in plastic and sectioned for light and electron microscopy. Hyperthyroidism stimulated a significant increase in heart rate, oxygen consumption, and systolic blood pressure. Propranolol was effective in normalizing the heart rate of hyperthyroid rats, but did not affect oxygen consumption or blood pressure. Both left and right ventricular weight increased similarly in thyroid and thyroid-propranolol treated animals, but right ventricular mass increased more than left ventricular mass in both groups. The majority (21 of 24) of right ventricles from thyroid and thyroid-propranolol treated animals had multifocal areas of histologically detected fibrosis. Left ventricular fibrosis was absent or minimal in both hyperthyroid groups. Neither left nor right ventricular fibrosis was observed in control or propranolol only treated animals. We conclude that beta adrenergic stimulation is unnecessary for thyroid induced cardiomegaly, and excess thyroid hormones induce right ventricular fibrosis which is not prevented by propranolol.

Animals↗
PubMed1977

[Bi-ventricular endo-myocardial fibrosis (author's transl)].

Bi-ventricular endo-mycardial fibrosis was diagnosed in two European women. Clinically there was severe cardiac insufficiency in the presence of only moderate radiological cardiac enlargement. Haemodynamically there was restricted filling, but otherwise normal systolic ventricular function. The diagnosis depended on the angio-cardiographic demonstration of a small, globular left ventricular chamber with a tubular narrowed right ventricle with a thickened wall, particularly at the apex. In one patient the endo-myocardial fibrosis was also demonstrated by echocardiography.

Adult↗
PubMed1991

Myocardial remodeling and pathologic hypertrophy.

The hallmark of myocardial hypertrophy associated with congestive failure is interstitial fibrosis. How does the fibrosis develop, and what can be done about it? Hormonal and hemodynamic factors are examined. Experimental studies with ACE inhibitors or aldosterone receptor antagonists suggest that the fibrosis may be prevented or reversed.

Animals↗
PubMed1996

Cardiac structure and function in renal disease.

Cardiac death secondary to ischaemia, but not necessarily associated with coronary lesions, is the leading cause of death in uraemic patients. This article reviews recent findings that demonstrate abnormalities of cardiac structure which have a bearing on ischaemia tolerance. These abnormalities comprise the following: (1) left ventricular hypertrophy not fully explained by increased mean arterial pressure, (2) interstitial fibrosis and (3) abnormalities of myocardial microvasculature, i.e. capillary rarefaction and arteriolar-wall thickening.

Endomyocardial Fibrosis↗
PubMed1991

Mechanisms of cardiac hypertrophy and injury--possible role of protein kinase C activation.

To examine the molecular mechanisms by which mechanical stimuli induced cardiac hypertrophy and injury, we cultured rat neonatal cardiocytes in deformable dishes and imposed an in vitro mechanical load by stretching the adherent cells. Myocyte stretching increased total cell RNA content and mRNA levels of c-fos. Marked accumulation of c-fos mRNA followed increases in intracellular Na+ and protein kinase C activation. The accumulation of c-fos mRNA by cardiocyte stretching was suppressed by protein kinase C inhibitors but not by stretch channel blockers. Moreover, myocyte stretching increased inositol phosphate levels, and activation of protein kinase C by phorbolesters stumulated the expression of c-fos. We also examined TGF beta expression in the heart. TGF beta is known to be stimulated by protein kinase C activation, and the mRNA level of TGF beta was increased in in vivo heart by pressure overload. Furthermore, collagen synthesis was stimulated by TGF beta in cultured fibroblasts from hearts. These findings suggest that hemodynamic overload may stimulate cardiac hypertrophy and induce cardiac injury (fibrosis) through protein kinase C activation.

Animals↗
PubMed2007

Patchy myocardial fibrosis 20 years after radiation therapy.

We describe a case of a young woman diagnosed with Ewings sarcoma at age 8 and treated with adriamycin and radiation therapy. Twenty years later the patient has a cardiomyopathy and a focal area of patchy infiltration of fibrotic tissue along the left ventricle and atrium. Although fibrosis due to radiation exposure has been demonstrated on biopsy and autopsy studies, we are not aware of previous reports of echocardiographic demonstration of this finding. The most likely explanation for the fibrosis location is the left posterolateral direction of the radiation beam.

Adult↗
PubMed1990

Myocarditis and myocardial interstitial fibrosis in constrictive pericarditis--an extended pathological spectrum?

We performed endomyocardial biopsy in six patients with constrictive pericarditis, revealing the presence of myocarditis and myocardial interstitial fibrosis in all regardless of the endocardial thickening. These findings suggest that the presence of endomyocardial involvement in the setting of restrictive heart disease should not be deemed specific for endomyocardial fibrosis when the clinical evaluation suggests constrictive pericarditis.

Endomyocardial Fibrosis↗
PubMed1995

Toward the biochemical assessment of myocardial fibrosis in hypertensive patients.

The serum concentrations of amino-terminal procollagen type III and carboxy-terminal procollagen type I-derived peptides, which have been proposed as useful markers of the tissue synthesis of collagen types III and type I, respectively, were abnormally increased in patients with essential hypertension and became normal after angiotensin-converting enzyme (ACE) inhibition. An association was found between baseline serum concentrations of these peptides and left ventricular hypertrophy, diastolic dysfunction, and ventricular arrhythmias in hypertensive patients. On the other hand, increased serum concentration of the carboxy-terminal procollagen type I-derived peptide was found in spontaneously hypertensive rats compared with normotensive Wistar-Kyoto control rats. An association was found between the serum concentration of this peptide and the extent of myocardial fibrosis and the hydroxyproline concentration in the left ventricle of spontaneously hypertensive rats. It is proposed that procollagen-derived peptides in serum may be markers of exaggerated collagen tissue synthesis involved in hypertensive myocardial fibrosis.

Animals↗
PubMed1991

Hypertrophy, fibrosis and diastolic dysfunction in early canine experimental hypertension.

To examine the relations among hypertrophy, fibrosis and diastolic performance in early experimental hypertension, 18 control dogs and 12 dogs with experimental left ventricular hypertrophy were studied. Diastolic function was impaired in dogs with left ventricular hypertrophy, with decreased Doppler early to atrial inflow velocity ratio (E/A) (1.35 versus 1.72), increased atrial filling fraction (35% versus 29%), decreased sonomicrometric peak rates of wall thinning (-2.01 versus -3.37 liters/s) and filling (4.33 versus 6.64 liters/s) and prolonged time constant of isovolumetric relaxation (tau; 34.3 versus 28.1 ms). Neither chamber stiffness (k; P = AekV) nor passive elastic stiffness (E; E = k sigma, where sigma = stress) was increased. At postmortem examination, the hypertensive left ventricle weighed significantly more than normal (116 versus 80 g; p less than 0.01) and had greater muscle fiber diameter at endocardial and epicardial sampling sites in the apical free wall, basal free wall and septum (mean diameter 50 +/- 8 microns in hypertensive dogs, 37 +/- 8 microns in normal dogs; p less than 0.01). In contrast, neither percent fibrosis (1.2 +/- 0.8 versus 0.9 +/- 0.6 in normal dogs) nor fibrotic volume (1.21 +/- 0.63 versus 0.72 +/- 0.42%/g in normal dogs) was significantly increased. Peak volumetric filling rate was inversely related to fiber diameter (r = -0.74, p less than 0.001), although no variable of left ventricular function was significantly related to percent or volume fibrosis (all r less than 0.60, all p greater than 0.05). Thus, diastolic dysfunction may exist in the setting of hypertrophy without significant fibrosis. Increased myocyte size was associated with early diastolic filling abnormalities characteristic of the hypertensive left ventricle. Fibrosis appears to be a less important determinant of diastolic performance.

Animals↗
PubMed1993

Cyclosporine A has no direct effect on collagen metabolism by cardiac fibroblasts in vitro.

BACKGROUND: Cyclosporine A has been implicated in the pathogenesis of myocardial interstitial fibrosis observed in heart transplant recipients. However, other confounding variables such as posttransplantation hypertension and rejection episodes may also be responsible for interstitial fibrosis development and associated abnormalities in ventricular diastolic function. Therefore, we examined whether cyclosporine A directly or indirectly affects fibrillar collagen metabolism by cardiac fibroblasts in vitro. METHODS AND RESULTS: Rat cardiac fibroblasts were isolated by collagenase digestion. Subconfluent cultures were then maintained (24 hours) in serum-containing or serum-free medium before addition of cyclosporine A (50-1,000 ng/mL). After an additional 24 hours, total procollagen synthesis, accumulation, and degradation were analyzed by measuring hydroxyproline content in the cell monolayer and in the ethanol-soluble and ethanol-precipitable fractions of the culture medium. mRNA levels for alpha 1(I) and alpha 1(III) procollagen polypeptides were assessed 2, 6, 12, and 24 hours after cyclosporine A treatment using Northern blot analysis. The results were compared with control cultures maintained in the absence of cyclosporine A. There were no differences in procollagen gene expression, total procollagen synthesis, accumulation, or degradation in cardiac fibroblasts treated directly with cyclosporine A, in concentrations up to 1,000 ng/mL, compared with untreated cells. In additional experiments, we examined whether cyclosporine A might stimulate the production of collagen regulatory substances by cardiac myocytes in culture. However, addition of conditioned media from neonatal myocytes maintained in the presence and absence of cyclosporine A (1,000 ng/mL) also had no effect on collagen deposition by cardiac fibroblasts. CONCLUSIONS: We conclude that cyclosporine A has no direct effect on collagen metabolism by cultured cardiac fibroblasts in vitro. In addition, we have excluded a paracrine effect of ventricular myocytes on collagen production in the presence of cyclosporine A. These results suggest that factors other than cyclosporine A are responsible for the interstitial fibrosis observed in cardiac allografts.

Animals↗
PubMed2004

Low coronary perfusion pressure is associated with endocardial fibrosis in a rat model of volume overload cardiac hypertrophy.

UNLABELLED: Left ventricular hypertrophy following volume overload is regarded as an example of cardiac remodeling without increased fibrosis accumulation. However, infarction is associated with increased fibrosis within the noninfarcted, hypertrophied myocardium, particularly in the subendocardial regions. It is conceivable to suppose that, as also occurs postinfarction, low coronary driving pressure may also interfere with accumulation of myocardial fibrosis following aortocaval fistula. PURPOSE: To investigate the role of acute hemodynamic changes in subsequent deposition of cardiac fibrosis in response to aortocaval fistula. METHOD: Aortocaval fistula were created in 4 groups of Wistar rats that were followed over 4 and 8 weeks: aortocaval fistula 4 and aortocaval fistula 8 (10 rats each) and their respective controls (sham-operated controls - Sh), Sh4 and Sh8 (8 rats each). Hemodynamic measurements were performed 1 week after surgery. Hypertrophy and fibrosis were quantified by myocyte diameter and collagen volume fraction at the end of follow up. RESULT: Compared with Sh4 and Sh8, pulse pressure, left ventricular end-diastolic pressure, and +dP/dt were higher in aortocaval fistula 4 and aortocaval fistula 8, but -dP/dt was similar. Coronary driving pressure (mm Hg), used as an estimate of perfusion pressure, was lower in aortocaval fistula 8 (52.6 +/- 4.1) than in Sh8 (100.8 +/- 1.3), but comparable between aortocaval fistula 4 (50.0 +/- 8.9) and Sh4 (84.8 +/- 2.3). Myocyte diameter was greater in aortocaval fistula 8, whereas interstitial and subendocardial fibrosis were greater in aortocaval fistula 4 and aortocaval fistula 8. Coronary driving pressure correlated inversely and independently with subendocardial fibrosis (r(2) = .86, P <.001), whereas left ventricular systolic pressure (r(2) = 0.73, P = .004) and end-diastolic pressure (r(2) = 0.55, P = 012) correlated positively and independently with interstitial fibrosis. CONCLUSION: Coronary driving pressure falls and ventricular pressures increase early after aortocaval fistula and are associated with subsequent myocardial fibrosis deposition.

Animals↗